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Mark J L Hocking1

  • 1Gladesville Veterinary Hospital, 449 Victoria Road, Gladesville, NSW 2111, Australia. mark.j.hocking@hotmail.com

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Myofascial trigger points (TrPs) cause pain and dysfunction. This research proposes that TrPs stem from central nervous system changes in alpha-motoneuron function, not local motor endplate issues.

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Area of Science:

  • Neurology
  • Physiology
  • Musculoskeletal Medicine

Background:

  • Myofascial trigger points (TrPs) are focal points of tenderness associated with taut muscle bands.
  • TrPs are a frequent cause of pain and motor dysfunction in humans and other vertebrates.
  • The pathophysiology, etiology, and treatment of TrPs lack universal consensus.

Purpose of the Study:

  • To review and extend a previously published hypothesis on the pathophysiology of TrPs.
  • To propose a novel understanding of TrP pathogenesis.
  • To challenge existing theories centered on local motor endplate dysfunction.

Main Methods:

  • Review of existing literature on myofascial trigger points.
  • Extension of the author's "Trigger Points and Central Modulation-A New Hypothesis."
  • Theoretical modeling of central nervous system modulation of alpha-motoneuron function.

Main Results:

  • The hypothesis posits that TrPs result from sustained plateau depolarization in alpha-motoneurons.
  • This central nervous system-maintained global change in alpha-motoneuron function is proposed as the underlying mechanism.
  • Local motor endplate dysfunction is suggested as a less likely cause of TrP pathogenesis.

Conclusions:

  • The central modulation hypothesis offers a new framework for understanding TrP pathophysiology.
  • Sustained alpha-motoneuron depolarization is proposed as the primary driver of TrP development.
  • Further research is warranted to validate the proposed central mechanisms in TrP etiology.